Mild Traumatic Brain Injury Induces Mitochondrial Calcium Overload and Triggers the Upregulation of NCLX in the Hippocampus
Traumatic brain injury (TBI) is brain damage due to external forces. Mild TBI (mTBI) is the most common form of TBI, and repeated mTBI is a risk factor for developing neurodegenerative diseases. Several mechanisms of neuronal damage have been described in the cortex and hippocampus, including mitoch...
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-02-01
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| Series: | Antioxidants |
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| Online Access: | https://www.mdpi.com/2076-3921/12/2/403 |
| _version_ | 1797622722215280640 |
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| author | Rodrigo G. Mira Rodrigo A. Quintanilla Waldo Cerpa |
| author_facet | Rodrigo G. Mira Rodrigo A. Quintanilla Waldo Cerpa |
| author_sort | Rodrigo G. Mira |
| collection | DOAJ |
| description | Traumatic brain injury (TBI) is brain damage due to external forces. Mild TBI (mTBI) is the most common form of TBI, and repeated mTBI is a risk factor for developing neurodegenerative diseases. Several mechanisms of neuronal damage have been described in the cortex and hippocampus, including mitochondrial dysfunction. However, up until now, there have been no studies evaluating mitochondrial calcium dynamics. Here, we evaluated mitochondrial calcium dynamics in an mTBI model in mice using isolated hippocampal mitochondria for biochemical studies. We observed that 24 h after mTBI, there is a decrease in mitochondrial membrane potential and an increase in basal matrix calcium levels. These findings are accompanied by increased mitochondrial calcium efflux and no changes in mitochondrial calcium uptake. We also observed an increase in NCLX protein levels and calcium retention capacity. Our results suggest that under mTBI, the hippocampal cells respond by incrementing NCLX levels to restore mitochondrial function. |
| first_indexed | 2024-03-11T09:14:16Z |
| format | Article |
| id | doaj.art-b535e7ccff1e46bf82dba1a9f5d1f8a4 |
| institution | Directory Open Access Journal |
| issn | 2076-3921 |
| language | English |
| last_indexed | 2024-03-11T09:14:16Z |
| publishDate | 2023-02-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Antioxidants |
| spelling | doaj.art-b535e7ccff1e46bf82dba1a9f5d1f8a42023-11-16T18:47:43ZengMDPI AGAntioxidants2076-39212023-02-0112240310.3390/antiox12020403Mild Traumatic Brain Injury Induces Mitochondrial Calcium Overload and Triggers the Upregulation of NCLX in the HippocampusRodrigo G. Mira0Rodrigo A. Quintanilla1Waldo Cerpa2Laboratorio de Función y Patología Neuronal, Departamento de Biología Celular y Molecular, Facultad de Ciencias Biológicas, Pontifica Universidad Católica de Chile, Santiago 8331150, ChileLaboratory of Neurodegenerative Diseases, Universidad Autónoma de Chile, Santiago 8910060, ChileLaboratorio de Función y Patología Neuronal, Departamento de Biología Celular y Molecular, Facultad de Ciencias Biológicas, Pontifica Universidad Católica de Chile, Santiago 8331150, ChileTraumatic brain injury (TBI) is brain damage due to external forces. Mild TBI (mTBI) is the most common form of TBI, and repeated mTBI is a risk factor for developing neurodegenerative diseases. Several mechanisms of neuronal damage have been described in the cortex and hippocampus, including mitochondrial dysfunction. However, up until now, there have been no studies evaluating mitochondrial calcium dynamics. Here, we evaluated mitochondrial calcium dynamics in an mTBI model in mice using isolated hippocampal mitochondria for biochemical studies. We observed that 24 h after mTBI, there is a decrease in mitochondrial membrane potential and an increase in basal matrix calcium levels. These findings are accompanied by increased mitochondrial calcium efflux and no changes in mitochondrial calcium uptake. We also observed an increase in NCLX protein levels and calcium retention capacity. Our results suggest that under mTBI, the hippocampal cells respond by incrementing NCLX levels to restore mitochondrial function.https://www.mdpi.com/2076-3921/12/2/403traumatic brain injurymitochondrial calciumNCLXhippocampus |
| spellingShingle | Rodrigo G. Mira Rodrigo A. Quintanilla Waldo Cerpa Mild Traumatic Brain Injury Induces Mitochondrial Calcium Overload and Triggers the Upregulation of NCLX in the Hippocampus Antioxidants traumatic brain injury mitochondrial calcium NCLX hippocampus |
| title | Mild Traumatic Brain Injury Induces Mitochondrial Calcium Overload and Triggers the Upregulation of NCLX in the Hippocampus |
| title_full | Mild Traumatic Brain Injury Induces Mitochondrial Calcium Overload and Triggers the Upregulation of NCLX in the Hippocampus |
| title_fullStr | Mild Traumatic Brain Injury Induces Mitochondrial Calcium Overload and Triggers the Upregulation of NCLX in the Hippocampus |
| title_full_unstemmed | Mild Traumatic Brain Injury Induces Mitochondrial Calcium Overload and Triggers the Upregulation of NCLX in the Hippocampus |
| title_short | Mild Traumatic Brain Injury Induces Mitochondrial Calcium Overload and Triggers the Upregulation of NCLX in the Hippocampus |
| title_sort | mild traumatic brain injury induces mitochondrial calcium overload and triggers the upregulation of nclx in the hippocampus |
| topic | traumatic brain injury mitochondrial calcium NCLX hippocampus |
| url | https://www.mdpi.com/2076-3921/12/2/403 |
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